[Effect of overexpression of aldehyde dehydrogenase family member A2 on hypertrophic growth and proliferation of cardiomyocytes].

Retinoic acid signaling pathway plays a role in regulating vertebrate development, cell differentiation, and homeostasis. As a key enzyme that catalyzes the oxidation of retinal to retinoic acid, aldehyde dehydrogenase 1 family member A2 (Aldh1a2) is involved in cardiac development, while whether it functions in heart diseases remains to be studied. In this study, we infected primary cardiomyocytes with adenovirus overexpressing <i>Aldh1a2</i> (Ad-Aldh1a2) to explore the effects of <i>Aldh1a2</i> overexpression on the biological function of cardiomyocytes. The results showed that the infection with Ad-Aldh1a2 realized the overexpression of <i>Aldh1a2</i> in cardiomyocytes. Compared with the control group infected with Ad-GFP, the cardiomyocytes infected with Ad-Aldh1a2 showcased significantly increased size and up-regulated expression levels of the atrial natriuretic factor gene (<i>ANF</i>), brain natriuretic peptide gene (<i>BNP</i>), and β<i>-</i>myosin heavy chain (<i>β</i>-<i>MHC</i>). In addition, 5-ethynyl-2'-deoxyuridine (EdU) incorporation assay demonstrated that <i>Aldh1a2</i> overexpression increased the proportion of cardiomyocytes with positive EdU signals and upregulated the expression levels of proliferation-related genes cyclin D2 (<i>Ccnd2</i>) and budding uninhibited by benzimidazole 1 (<i>Bub1</i>). The above data indicated that overexpression of <i>Aldh1a2</i> induced hypertrophic growth and proliferation of cardiomyocytes. This study provides a basis for further understanding the function of Aldh1a2 in heart diseases and developing therapies for heart diseases.